1/78. flour contamination as a source of lead intoxication.CASE REPORT: A 43-year-old man was hospitalized because of severe anemia and recurrent bouts of abdominal pain over 20 days. There was no known occupational exposure to toxins. Concomitantly, the patient's father complained of having the same symptoms. Familial lead poisoning was diagnosed when all 6 family members tested had high blood leads (31-64 micrograms/dL). RESULTS: Following detailed examination of the potential sources common to all members of the household, the cause of poisoning was determined to be corn flour containing 38.7 mg/g lead. physicians are reminded to consider lead poisoning in the differential diagnosis of individuals with unexplained symptoms, particularly those of abdominal discomfort and anemia.- - - - - - - - - - ranking = 1keywords = abdominal pain, pain (Clic here for more details about this article) |
2/78. An unusual cause of recurrent abdominal pain.abdominal pain is a common complaint with diverse etiologies. We describe an unusual case of recurrent abdominal pain in an adult due to lead poisoning, a condition usually associated with childhood. A previously healthy 42-yr-old man presented with 2 days of severe crampy abdominal pain and a 1-month history of constipation. physical examination was remarkable for diffuse abdominal pain but peritoneal signs were not present. Blood tests were remarkable for hematocrit of 33 and mean cell volume of 78, with ovalocytes and basophilic stippling on blood smear. Abdominal x-ray showed stool throughout the colon and a nonspecific bowel gas pattern. The patient was treated with intravenous fluids and enemas, and his symptoms resolved within 2 days. Repeat history taking revealed he had been stripping paint from an old Victorian house in the preceding few months. He was discharged after a blood lead level was obtained. Before his clinic appointment he was readmitted 2 days later with recurrent abdominal pain. His blood lead level was elevated at 110 microg/dl (toxic range). After consultation with the occupational health and safety Administration and local poison control service, he was treated with intravenous calcium edetate disodium and intramuscular dimercaprol. He was asymptomatic at discharge, with a level of 56 microg/dl. Two weeks later, a repeat level was elevated at 72 microg/dl, for which he received a 3-wk course of oral dimercaptosuccimer. Subsequent levels were unremarkable, and the patient remains asymptomatic. abdominal pain secondary to lead poisoning in adults is uncommon. This case highlights the importance of taking a detailed occupational history and appropriately using "routine" blood tests to diagnose a rare condition that presented with a common complaint.- - - - - - - - - - ranking = 8.1428617061916keywords = abdominal pain, pain (Clic here for more details about this article) |
3/78. lead poisoning after gunshot wound.CONTEXT: Despite the absence of symptoms in the majority of patients carrying lead bullet fragments in their bodies, there needs to be an awareness of the possible signs and symptoms of lead intoxication when bullets are lodged in large joints like knees, hips and shoulders. Such patients merit closer follow-up, and even surgical procedure for removing the fragments. OBJECTIVE: To describe a patient who developed clinical lead intoxication several years after a gunshot wound. DESIGN: Case report. CASE REPORT: A single white 23-year-old male, regular job as a bricklayer, with a history of chronic alcohol abuse, showed up at the emergency department complaining of abdominal pain with colic, weakness, vomiting and diarrhea with black feces. All the symptoms had a duration of two to three weeks, and had been recurrent for the last two years, with calming during interval periods of two to three weeks. Abdominal radiograms showed a bullet lodged in the left hip, with a neat bursogram of the whole synovial capsule. A course of chelating treatment using calcium versenate (EDTACaNa2) intravenously was started. After the chelation therapy the patient had recurrence of his symptoms and a radical solution for the chronic mobilization of lead was considered. A hip arthroplasty procedure was performed, leading to complete substitution of the left hip.- - - - - - - - - - ranking = 1keywords = abdominal pain, pain (Clic here for more details about this article) |
4/78. lead poisoning from a retained bullet: a case report and review.A 47-year-old man with a prior gunshot wound presented with arthritis, constipation, abdominal pain, and weight loss. Arthrocentesis did not reveal the cause of the arthritic complaints, but lead poisoning was suspected and confirmed. We present this case along with a short review of the literature pertaining to this often overlooked and reversible cause of lead poisoning.- - - - - - - - - - ranking = 1keywords = abdominal pain, pain (Clic here for more details about this article) |
5/78. Acute elevation of blood lead levels within hours of ingestion of large quantities of lead shot.BACKGROUND: Ingestion of elemental lead foreign bodies is felt to have a low risk of clinically significant lead absorption unless gastrointestinal pathology and/or prolonged transit time are present. We present a case of ingestion of a large quantity of small diameter lead shot accompanied by rapid elevation of blood lead levels. CASE REPORT: A 5 1/2-year-old previously healthy girl was found eating the pellets from an ankle weight. She vomited and complained of abdominal pain. In the emergency department, she had no complaints and normal vital signs. An abdominal X-ray showed thousands of small, round, metallic density objects in the stomach. Her white blood cell count was 14,700/mm3, and the hemoglobin, mean corpuscular volume, free erythrocyte protoporphyrin, zinc protoporphyrin, biochemistry panel 21, and urinalysis were normal. She had no prior lead level for comparison. Whole-bowel irrigation was begun and she passed over 11 stools with pellets as well as other foreign bodies (erasers, bead, etc.) in the first 24 hours. Pellets were still seen on X-ray the following day so she received a high-fiber diet and bisacodyl tablets 10 mg/d. On hospital day 2, her admission blood lead (drawn 13 hours after ingestion) was reported as 57 microg/dL (2.7 microm/L) and chelation was begun with oral 2,3-dimercaptosuccinic acid 10 mg/kg 3x/d for 5 days, then 2x/d for 14 days. Her peak measured lead level was 79 microg/dL approximately 36 hours after ingestion. She excreted 2,273 microg lead in the urine during her first 24 hours of chelation. Her blood lead dropped to 14.3 microg/dL by the end of chelation. She did not develop any apparent signs of lead poisoning. CONCLUSION: Acute elevations of blood lead concentrations may occur rapidly after ingestion of multiple small elemental lead objects.- - - - - - - - - - ranking = 1keywords = abdominal pain, pain (Clic here for more details about this article) |
6/78. Poorly controlled hypertension in a painter with chronic lead toxicity.In 1984, a 56-year-old house painter developed intractable pain in his back and other joints. After several unrevealing medical work-ups, he was found to have a high blood lead level (122 microg/dL); he has a history of scraping and sanding lead paint without adequate protective measures. The patient was hospitalized and chelated with EDTA four times over the next 5 years; each time he felt better at the end of his treatment, but he returned to largely the same working conditions. He developed hypertension in April 1989, underwent a final chelation, and retired. He was subsequently followed on a regular basis with repeated measurement of lead levels in blood and bone (using a K-x-ray fluorescence instrument) as well as clinical parameters. In 1995 his blood pressure became difficult to control despite a sequential increase in his antihypertensive medication dosages and the addition of new medications. In 1997 he began calcium supplementation and a high-calcium diet; his blood pressure declined markedly, allowing him to taper off of two of his four antihypertensive medications. This case demonstrates an occupational activity (construction) that has now become the dominant source of lead exposure for U.S. adults, the importance of a good occupational history to suspecting and making a diagnosis, the possible outcomes of chronic lead toxicity, and the importance of preventing further exposure and using proper methods to treat acute toxicity. It also highlights a current major etiologic question, that is, whether and to what degree lead exposure contributes to the development of hypertension, and raises the issue of whether lead-induced hypertension constitutes a subset of hypertension that is especially amenable to therapy with dietary calcium.- - - - - - - - - - ranking = 0.33334398111372keywords = pain (Clic here for more details about this article) |
7/78. A presumptive case of lead poisoning in a brass-worker's child.A one-year-old male child was admitted with the complaints of vomiting and irritability for 4 days, haematemesis and melaena for one day and had generalised tonic convulsions on the day of admission. Examination revealed exaggerated reflexes with group II coma. Blood film showed basophilic shippling. Straight x-ray showed lead lines in the metaphyses of ribs, humerii, scapulae, iliac crests and upper ends of femurs. The boy's father was an employee of brass industry where brass alloys used cotained lead in substantial amount. A presumptive case of lead poisoning (as diagnosed) was treated symptomatically. Chelating agent was called for but the patient left. In the present case the hands of the child were contaminated with lead dust brought home by his father either in person or in clothings. The child used his hands constantly in his mouth to get poisoned by lead.- - - - - - - - - - ranking = 0.00022395448268869keywords = upper (Clic here for more details about this article) |
8/78. Occupational and take-home lead poisoning associated with restoring chemically stripped furniture--california, 1998.The Occupational lead poisoning Prevention Program (OLPPP) of the california Department of health services and a county health department investigated cases of lead poisoning in six furniture workers and their families in 1998. The investigation, initiated after a blood test of a worker's child revealed an elevated blood lead level (BLL), found that lead remaining in previously painted or coated stripped wood was carried from the workplace on clothes and shoes and was the source of the child's lead exposure and subsequent poisoning. Employers in industries in which workers restore or build using stripped wood should assess lead exposure and, when necessary, should establish a comprehensive lead safety program.- - - - - - - - - - ranking = 0.047620568730531keywords = pain (Clic here for more details about this article) |
9/78. Fatal pediatric lead poisoning--New Hamphshire, 2000.Fatal pediatric lead poisoning is rare in the united states because of multiple public health measures that have reduced blood lead levels (BLLs) in the population. However, the risk for elevated BLLs among children remains high in some neighborhoods and populations, including children living in older housing with deteriorated leaded paint. This report describes the investigation of the first reported death of a child from lead poisoning since 1990 (1). The investigation implicated leaded paint and dust in a home environment as the most likely source of the poisoning. lead poisoning can be prevented by correcting lead hazards, especially in older housing, and by screening children at risk according to established guidelines (2).- - - - - - - - - - ranking = 0.095241137461062keywords = pain (Clic here for more details about this article) |
10/78. Peripheral neuropathy in chronic occupational inorganic lead exposure: a clinical and electrophysiological study.BACKGROUND AND OBJECTIVES: Traditionally the neuromuscular disorder associated with lead poisoning has been purely motor. This study assessed peripheral nerve function clinically and electrophysiologically in 46 patients with neuropathic features out of a total population of 151 workers with raised blood and/or urinary lead concentrations. RESULTS: Average duration of occupational exposure for the neuropathic group ranged from 8-47 years (mean 21.7). Their mean blood lead concentration (SD) was 63.9 (18.3) microg/dl (normal <40), urinary lead 8.6 (3.3) microg/dl (normal<5.0), urinary coproporphyrins 66.7 (38.4) microg/g creatinine (20-80), urinary aminolaevulinic acid 1.54 (0.39) mg/g creatinine (0.5-2.5). All 46 had distal paraesthesiae, pain, impaired pin prick sensation, diminished or absent ankle jerks, and autonomic vasomotor or sudomotor disturbances. Reduced vibration sensation and postural hypotension were present in all 20 studied. None of these 46 patients had motor abnormalities. Motor conduction velocity and compound muscle action potential amplitudes were normal, with marginally prolonged distal motor latencies. Sensory nerve action potential amplitudes lay at the lower end of the normal range, and the distal sensory latencies were prolonged. No direct correlation was found between the biochemical variables, and the clinical or electrophysiological data. CONCLUSIONS: One additional patient was seen with shorter term exposure to lead fumes with subacute development of colicky abdominal pain, severe limb weakness, and only minor sensory symptoms. Unlike the patients chronically exposed to lead, he had massively raised porphyrins (aminolaevulinic acid 21 mg/g creatinine, coproporphyrins 2102 microg/g creatinine). patients with unusually long term inorganic lead exposure showed mild sensory and autonomic neuropathic features rather than the motor neuropathy classically attributed to lead toxicity. It is proposed that the traditional motor syndrome associated with subacute lead poisoning is more likely to be a form of lead induced porphyria rather than a direct neurotoxic effect of lead.- - - - - - - - - - ranking = 1.0476205687305keywords = abdominal pain, pain (Clic here for more details about this article) |
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